This invention relates to a heart display system and more particularly to a system which simulates the electrophysiological process in the heart and displays a representation of the simulated process.
The operation of heart depends on a process of polarization and depolarization in nervous pathways and muscular tissue in the heart.
Living cells are made up of an ion enclosing membrane, which in its resting state has a -90 millivolt difference in voltage between the inner and outer wall. In this condition the cell is considered polarized. When excited the cell depolarizes by the dielectric strength of the wall breaking down and ions flowing across the barrier. This causes a contraction of muscular cells. But, particularly in cardiac muscle and nervous conduction paths, a cell that depolarizes also triggers its neighbor to depolarize in a chain reaction until the entire nervous path or area of muscular tissue is involved. The chain reaction causes the depolarization to travel in a wave through the nervous pathways and the muscular tissue and in this manner electrical impulses are conducted through the heart. Cells remain depolarized for only a short period of time, called the refractory time, and then the cell wall barrier is again established with a restoration of a net flow of negative ions to the inner cell until a -90 mv equilibrium is reached. Only during the charged or polarized state is the cell capable of being activated or depolarized.
If a portion of the atrium, ventricle, or a conducting nervous path is depolarized that portion cannot conduct an impulse until it has recovered. If depolarized cells are in the line of conduction of new depolarization activity, the activity stops at the barrier comprising the depolarized cells.
A single normal heart contraction results from the spontaneous excitation of the cells in the upper right atrium called the sinus node. This particular node acts as a natural physiologic pacemaker of the heart and is influenced by the brain and nervous system of the body. Its electrical activity spreads throughout the atrium with a conduction velocity determined by the anatomy and chemical environment of the atrium at the time. The spread of the depolarization wave through the atrial walls causes the atrial muscle to contract and carry out the atrial pumping action. The speed of conduction, upon reaching the atrio-ventricular node (AV node) of the heart, considerably slows. After passing through the AV Node the activity proceeds through nervous fibers called the His bundle, the right and left bundle branches and then through many parallel exits to the ventricular myocardium. The depolarization wave then spreads through the muscular tissue of the ventricle to cause the ventricle to contract producing the ventricle pumping action. All of this activity is very fast compared to the rate of conduction through the AV node. Thus, the mechanical pumping of the ventricle is delayed from the pumping of the atrium to permit the atrium to contribute substantially to the filling of the ventricular chambers.
Many factors contribute to the rate of the heart and the conduction sequence of the normal heart, and many more factors become involved with abnormal and diseased hearts. Hearts can acquire concealed paths of conduction, or longitudinally diassociated paths resulting in two conduction paths where one normally exists. Conduction velocities and refractory periods can change radically with disease. Conduction blocks can take place so that activity will not proceed past certain barriers. Irritable cells can develop almost anywhere in the heart and start rhythmic depolarizations which can propagate throughout the heart producing pacemaker action conflicting with normal rhythm.
As indicated above, the activity of the heart normally originates from the sinus node. However, despite the origin of a beat, the activity spreads from an excited cell like a wave spreads from a stone splash in a pond, or more analogously, like falling dominos set up in close proximity. If neither neighbor on either side of a domino falls then the domino remains standing. If neither neighbor of a cell depolarizes, a cell remains quiescent, (except for a spontaneously depolarizing cell). If a domino is down and there is no path of dominos around the fallen or missing domino, activity will stop at the break. If there is a dead cell in a conducting link, or if the cell has not yet recovered by the time that new activity arrives, such activity will be blocked.
The sequence of normal cardiac activity involves a first atrial contraction followed closely by ventricular contraction at a rate depending upon physiologic needs. However, with irritable foci and/or diseased aberrant pathways, the electrical conduction sequence of the heart can assume bizarre sequences and rhythm, which can be dangerous. The characteristics of the heart's electrophysiologic conduction system and the resulting rhythms and arrhythmias can be very complex. It is often difficult or impossible to definitively identify the mechanisms actually responsible for specific arrhythmias seen on the patient's electrocardiogram.
At the present time physicians encountering difficult arrhythmias will order electrophysiologic studies of the patent. These studies involve monitoring the electrocardiagraphic voltages at multiple sites on the heart during electrical stimulation, which is meant to provoke or stop such arrhythmias. These studies may be carried out while the patient is affected by specific drugs. From these data the physician tries to create a series of diagrams which model the conduction system of the heart of the patient and yield the precise mechanisms involved. This is a time consuming process and lacks ease in testing postulated parameters and their possible variations.
As explained above, the electrophysiology of the heart is a relatively complex study. Medical students have difficulty in understanding the basic principles of cardiac conduction activity and resulting cardiac rhythms and the multiple variations that exist in this activity. Even the expert cardiac electrophysiologists has difficulty in visualizing the precise mechanisms possible in contributing to complex arrhythmias, particularly when there are multiple pathways in the heart with rate and interval dependent parameters.
The usual presentation of an arrhythmia problem includes slides or pictures of a multichannel ECG including intracardiac electrograms from different sites of the heart. Frequently these electrograms are accompanied by postulated ladder diagrams displaying the conduction sequence and pattern representing the rhythm. Comprehension of the presented rhythm requires careful examination of the whole picture with extensive consideration and thought aided by an accompanying oral presentation or written text. The learner frequently saves time by taking the authors explanation on faith, consequently sometimes learning only the superficial lesson without the subtile aspects that could later contribute to his intuitive grasp of cardiac rhythm variations encountered in practice.